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Respiration Flashcards

0
Q

Define tidal volume, respiratory rate and pulmonary ventilation rate

A

Tidal volume = normal volume expired on a breath (not forced)
Respiratory rate = breaths per minute
Pulmonary ventilation rate = air in and out in one minute = tidal volume x rr

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1
Q

States boyles law, Charles law and the universal gas law

A

Boyles law = pressure is inversely proportional to volume.
Charles law = pressure is directly proportional to temperature
Universal gas law= pressure x vol = temperature x gas constant

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2
Q

What is a meatus?

A

Channel formed by nasal conchae (turbinates) superior middle and inferior.

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3
Q

Define partial pressure, vapour pressure, tension and saturation vapour pressure.

A

Partial pressure - pressure (number of collisions of gas against a container) of just one gas in a mixture.
Vapour pressure - partial pressure of water above a surface of water
Tension - a gases’ tendency to escape a liquid
Saturation vapour pressure - the maximum pressure of water vapour in equilibrium with the liquid phase. Depends on temperature.

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4
Q

What is an olfactory region?

A

Region without as much mucous secretions for smell. Thick epithelia. Washed by serous secretions. Non olfactory have venous sinuses in LP that swell so that air only goes through 1/2 of nose

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5
Q

Describe 4 para nasal sinuses and their use

A

Sphenoidal
Ethmoidal
Maxillary
Frontal

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6
Q

Composition of glottis

A 
Plicae vocales (true) attached to the arytenoid cartilage (posterior to larynx and thyroid cartilage and superior to cricoid cartilage)
Vestibular folds (false)
In between in the rima glottidis
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7
Q

Cartilage in lower respiratory tract?

A

Trachea C shaped and fibroelastic membrane with trachealis.
Primary bronchi - ring
Secondary and tertiary have a crescent, plates or islands
Bronchioles - none

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8
Q

Upper and lower and resp portion?

A

Sternal angle/ glottis

Bronchioles to alveoli.

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9
Q

Describe differences in ribs

A

1atypical - only have inferior facet on head, shortest, broadest, most curved.
2 atypical - no prominent costal groove
3-8- typical
9-10 typical but fuse to costal cartilage which joins costal cartilage of rib above not the sternum.
11-12 atypical ribs don’t fuse to cartilage, lie in diaphragm, only superior facet present on head, no tubercle

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10
Q

Describe the structure of a rib and it’s articulations

A

Head, superior and inferior facets (articulate with Demi facets of vertebral bodies) separated with crest
Neck - tubercule inferior laterally which articulates with transverse facet of vertebrae. (Costotransverse joint)
Costal groove found inferior, arteriorly

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11
Q

What is the costal margin?

A

Where costal cartilages form a V towards the sternum

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12
Q

Describe the intercostal muscles function and innervation.

A

External (anterior and inferior), hands in pockets, raises ribs, inspiration
Internal (anteriorly) and innermost(laterally), 90 deg, depresses ribs, forced expiration.
Supplied by anterior rami of corresponding nerve

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13
Q

Describe the structure of the diaphragm

A

Muscle ribs start from ribs, arcuate ligaments (median, lateral and medial) ad right and left Cruz and go to the central tendon.

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14
Q

Describe the distribution of intercostal nerves arteries and veins and their roots and what the nerves supply. Including supply and drainage

A

Artery- anastomoses between aorta and internal thoracic artery.
Vein - drains into azygous vein (SVC) (some into internal thoracic vein)
Nerve - anterior rami, supplies muscles, skin and costal and cervical parietal pleura.
Found in costal groove and just superior to rib

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15
Q

Phrenic nerve innervation.

A

3,4,5

Diaphragm, sensory to mediastinal and diaphragmatic pleural and the pericardium. Both surfaces of diaphragm.

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16
Q

Describe the pleural cavity and the lines of pleural reflection

A

Costal, cervical, diaphragmatic and mediastinal

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17
Q

Describe the mediastinal and their contents

A

Superior mediastinum. Bounded superiorly by thoracic inlet, inferiorly by T4- angle of Louis/ pericardium. Contains oesophagus, tachea, muscles, phrenic nerve, deep and superior cardiac plexuses, arch of the aorta, thymus, SVC, vagus, muscles
Anterior mediastinum - chest wall and fibrous pericardium. Thymus in kiddies, long thoracic vein and artery, sternophrenic ligament
Posterior mediastinum - descending/thoracic aorta, azygous vein, oesophagus, thoracic duct, vagus nerve, splanchnic nerve, sympathetic veins and trunk

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18
Q

Locations of PV, PA and bronchus in right and left hilum

A 
Bronchi anterior
Veins posterior 3/2
Left artery superior
Right arteries (2) middle
Lymph nodes between veins
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19
Q

What is the rate of diffusion in the lungs usually limited by?

A

Not area, or pressure, diffusion barrier - 5 layers

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20
Q

Describe the properties of the mechanical system comprising the lungs, chest wall and diaphragm

A

Lungs: elastic tissues for recoil
Chest wall: draws chest out via pluera to increase AP
Diameter: contracts to draw chest down increasing sup/infer

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21
Q

Muscles in forced inhalation and expiration?

A

Inspiration: external costal, diaphragm, serratus anterior, pec minor, scalene, sternocleidomastoid
Expiration: innermost and internal intercostal muscles, abdominal muscles

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22
Q

Define functional residual capacity, residual volume, vital capacity and inspiratory capacity

A

Tidal vol - total volume breathed in and out on a normal breath/ displaced with no extra effort.
Inspiratory reserve vol- extra volume than can be inspired than normal
Exploratory reserve vol - extra vol that can be expired than normal
Inspiratory capacity - total amount that can be inhaled after a normal exhale.
Residual vol - air left in lungs after a forced expiration
Functional residual capacity- air left in lungs after a normal expiration
Vital capacity- maximal amount that can be inhaled from the RC

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23
Q

Serial dead space, physiological dead space and how these variables are measured

A

Serial dead space= non collapsible structures- bronchi upwards. Air in structures that do not take part in gas exchange - 150ml. (Conducting airway)

Measured via nitrogen washout, forced expiration, forced inspiration of 100% O2, amount of N2 measured and use to calculate volume.

Physiological dead space= serial dead space + alveolar dead space (gas in alveoli that can’t take place in gas exchange).
Looking at pO2 and pCO2 breathed out compared with normal alveolar pressures as alveolar air is dilated by dead space air.

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24
What is alveolar ventilation rate and how is it calculated?
Tidal volume - physiological dead space * respiratory rate
25
Define compliance of the lungs and how it is measured
Stretchiness of lung, higher means more stretch. | Change in vol/ change in pressure
26
Factors which affect compliance
Surface area. As surface area increases then compliance decreases. This is due to water tension. Surfactants decrease water tension so increase compliance
27
What is hysteresis?
No all energy put into stretching lungs on inspiration is released on recoil. Greatest when tidal vol is maximal.
28
Why do big bubbles eat little bubbles? (Or not)
Laplaces law = 2x SA/ radius = pressure High bubbles have a lower pressure so eat small bubbles. Surfactant decreases water tension so bub les are stabalised- less in big bubbles so a higher tension.
29
Factors which affect airway resistance and how resistance changes over a breathing cycle.
Poiseulles law. Resistance through a tube is inversely proportional to radius. Larger radius then lower resistance. Tubes narrow on expiration so more resistance. Compliance also affects how much we can inhale.
30
Describe spirometry
Measures FVC. Can link to a vitalograph to measure over time. Limited by compliance, for e of muscles and airway resistance
31
Describe FVC and FEV1.0
Force vital capacity and forced expiratory vol in one second | On vitalograph
32
Explain obstructive and restrictive patterns of spirometry.
Obstructive then lower fev e.g. Asthma | Resistrictive the lower FVC e.g. Fibrosis and chest wall probs
33
Explain inspiratory and expiratory flow volume loops and how they are affected by upper and lower airway obstructions
Peak flow meter PEFR Decrease in flow after peak flow (at higher vols) unless severe.
34
Describe the measurement of residual volume
Helium dilation - not taken into blood stream. Measure difference in conc.
35
Describe the measurement of transfer factor.
CO, only limited by diffusion barrier. Binds to haem readily. Measure differnces in conc for TF
36
State the solubility of O2 in body fluid
0.01mmol/l/kPA at 37
37
What are the normal values of alveolar and capillary pO2?
13.3 | 5kPa
38
Properties of haemoglobin that makes it good
``` Tetromer. Exists in two states. Tense hard to bind Relaxed easy to bind More PO2 then more R Highly reversible. Lower O2 at tissues so more delievered. High temp and H+ cause more T ```
39
Effects on the dissociate curve of a high temp/ fall in pH
Right left, harder to bind
40
Estimate rate of delivery of O2 to tissues at different capillary pO2s and pHs
Haem found at 2.2 mmol/ l and bind 4 O2. | Use graph and O2 saturation at different pressures
41
Factors affecting gas diffusion in alveoli
Thickness of barrier/ resistance to diffusion Partial Pressure gradient Area
42
How is the transfer factor obtained/ diffusion capacity
Vital capacity containing CO. Exhale, how much CO is there now? pCO in blood =0 and so all that can transfer will have. First 750ml is discarded. Helium used to measure dilution effects.
43
Reactions of CO2 in blood
CO2+H20 = HCO3 + H In mito, more HCO3 produced so equilibrium to left. Dissolved CO2 affects pH
44
What is the Henderson hasselbach equation a and calculate pH given pCO2 and HCO3
PH= pK (6.1) + log( HCO3/(CO2*0.23))
45
Factors affecting HCO3 conc
H+ reacts with haemoglobin so more HCO3 produced and leaves RBC via AE Kidney maintain long term via reabsoption
46
Buffering action of haem in RBC
High CO2 then H+ binds to HCO3 and haem | Low CO2 then Co2 reacts with H2O to form more H+/ dissociates from haem
47
Function of carb amino proteins
Binds to CO2 so that it cannot dissolve. This co2 therefore has no effect on pH. Transport molecules
48
Normal content of CO2 in arterial and venous blood
21.5mmol/l in arterial 23.5 mmol/l in venous Haem can bind more H+ without O2 in venous so blood can carry more CO2 without pH changing
49
State the proportion of CO2 travelling in various forms.
80% HCO3 11% carbamino 8% dissolves CO2
50
Define hypoxia hypocapnia, hyperventilation and hypoventilation
PCO2<8 Low CO2 (3.5?) RR 12-20
51
Effects on plasma pH of hypo and hyper ventilation and the result
Effects co2, effects pH. Acidosis- coma, seizures, arrhythmias, vomiting, nausea Alkalosis- fainting, dizziness, coma, free Ca decrease so tetany
52
Define respiratory acidosis and alkalosis, compensated respiratory acidosis and alkalosis
Due to over/ under ventilation/perfusion rise/fall in CO2 so pH effects. Compensated by kidney- removal of HCO3 or retention
53
Define metab acid/alk and compensated?
Due to metabolic cause e.g. Ketoacidosisis or lactic acidosis or antifreeze or vomiting. Compensated quickly by ventilation
54
Describe acute effects upon ventilation of falling pO2, increase in inspired pCO2 and falls in arterial plasma pH.
All increase
55
Location and function of central chemoreceptors. Roles if the cerebrospinal fluid (CSF) blood brain barrier and choroid plexus in the response
Medulla around CSF. Detect pH only affected by CO2 which freely diffuses but HCO3 does not. If increaesed/ decreased ventilation does not solve then HCO3 diffuse via choroid plexus to neutralise and stop.
56
Metabolic acidosis detection?
Peripheral as only change I'm HCO3??
57
Describe type 1 resp failure
Low O2 but normal or decreased CO2. Occurs when problems in ventilation/perfusion or diffusion barrier. E.g. Pneumonia, PE Breathlessness, central cyanosis, exercise intolerance
58
Describe type 2 resp failure
Low O2 me high Co2. Problems with ventilation e.g. Chest wall probs, COPD, asthma, opioids Acutely then breathlessness but compensation occurs and CSF equilibriates so driven by hypoxia. Can cause pulmonary hypertension due to contraction in response to hypoxia
59
How can arterial blood gases be measured?
Pulse oximetry
60
Describe ventilation/perfusion mismatch and diffusion impairment and how they can lead to type1. Outline the causes of each
Want to be 1 (0.8 is normal). | PE/ thicker barrier (pneumonia) means less perfusion so not all O2 breathed off
61
Describe how hypoventilation results in type 2 and outline its important causes
Fibrotic lung disease, COPD, emphysema (severe), severe asthma, scoliosis/ kyphosis
62
Define asthma and describe the nature of airflow obstruction in asthma
Chronic disease characterised by airway remodelling - thickening of SM and BM. Reversible airflow obstruction. Hypersensitivity/ increased airway responsiveness to a variety of stimuli. Damaged epithelium due to chronic inflammation More likely in females. Can be allergic (eosinophils, IgE and mast cells), asprin sensitive or occupational (farmers, welders and bakers)
63
Describe the pathophysiology of asthma
Mucins and hypersensitivity/ contraction and narrowing of airway make a reversible airflow obstruction. To maintain flow pressure must change (r4) (poiseuilles equation)
64
Describe the precipitating factors for asthma attack
ACh release- muscurinic agonist, prostaglandins, leukotrienes, histamine, cold air Allergens - dust mites, air pollution, fungal spores, HDM, pollens
65
Describe the signs and symptoms of asthma and their physiological basis
``` Dry cough- no infection- worse on exercise Respiratory wheeze Dispnoea Chest tightness Recession and tracheal tug Prolonged expiratory phase ```
66
Describe the tests used to assess the condition of a patient suspected of asthma and how they are interpreted
History- eczema, family history, prenatal smoking, occupation Examination- hyperesonant, barrel chest, Investigation- flow volume loop- restrictive, auscultation polyphonic wheeze. lower FEV/FVC or normal, lower PEFR- 12% increase in FEV with salbutamol. bronchial hyper responsiveness- bronchial challenge test e.g, histamine. FENO- released from inflammation. Allergy testing Sputum induction Exercise induced bronchoconstriction- pre and post spirometry.
67
Principles of treating asthma
Prevent- smoking, allergens, exercise, housing, cleaning B2 agonists Muscurinic antagonists -ipratropium (anticholinergic) Theophylline/ aminophylline (anti inflam) Corticosteroids and leukotrienes receptor antagonist . Acutely- IV drugs, interbate, ventilate, salbutamol and atrovent nebs, O2
68
Peripheral chemoreceptors location
Carotid and aortic bodies
69
Describe the major precipitating factors for asthmatic attacks
Lack of treatment adherence Respiratory virus infections associated with the common cold Exposure to allergen or triggering drug e.g. NSAIDS
70
Describe the main causes of COPD and the nature of airflow obstruction in COPD
Chronic bronchitis - inhaled irritants e.g. Smoking, cause chronic inflammation which damages muco-ciliary escillator, damages epithelium, increases mucous secretion with the result being narrowed airways Emphysema - loss of elastin leading to destruction of alveolar walls, irritants and inflammation Both are progressive and not fully reversible
71
Describe the signs and symptoms of COPD
Tachypnoea Cough dry or productive worse at night Infection Barrel chest, hyper resonant due to hyperinflation and air trapping Leaning forward- accessory muscles Reduced intensity breath sounds Reduced air entry, loss of elasticity and tissue breakdown increasing resistance and residual capacity. Possible wheeze May develop pulmonary hypertension, central cyanosis, Hypercapnia (flapping tremors. MRC Dyspnoea scale
72
Investigations of COPD patients
Cxr- hyper expansion - flat diaphragm, more than 6 ribs, increased anteroposterior diameter, hyperlucent lungs, signs of pneumonia/ pneumothorax, rule out other stuff. Pulse oximetry and ABG Lung function tests- ratio under 70% and limited reversibility. Reduced FEV
73
Management of COPD patients
ACh blockers Ipratropium, bronchodilators- salbutamol. Stop smoking Exercise Education Surgery- remove bullae from emphysema, lung transplant, Pneumonia vaccine Oxygen therapy- prevent hypertension and relieve symptoms (not if breathless) long as possible, portable or just intermittent Corticosteroid- decrease inflammation Ventilate Pulmonary rehab- increase exercise capacity
74
Outline normal flora of the GI tract
Viridens streptococci (a haemolytic), anaerobes, neisseria spp, Candida albicans Sometimes: Strep pneumoneai, pyrogens, h influenzae, Rare: E. coli, pseudomonas
75
Natural defenses of respiratory tract against infection
Muco ciliary escalator Lymphatics, alveolar macrophages, IgA and IgG secreted Cough and sneeze
76
Main infectious diseases of upper respiratory tract and the organisms commonly causing these infections
``` Sinusitis Parotitis Tracheitis Laryngitis Pharyngitis Otitis media Rhinitis - cold Epiglottitis ``` RSV Coronovirus Influenza Rhinovirus ``` May lead to bacterial infection Meningitis Mastoiditis Brain abcess Common with sinusitis or Otitis media ```
77
Define the term pneumonia and distinguish between acute and chronic
Pneumonia- infection of lung parenchyma with consolidation (not compressible) and exudate Acute/ lobar- one lobe affected normally CA and strep pneumoniae. May lead to emphyma, lung abscess or bronchiectasis (widened) Chronic - bronchial- multiple lobes affected, widespread/ patchy consolidation, starts in bronchi, often hospital aquired, may cause heart failure, viral infections.
78
Describe the infectious aetiology of acute community acquired and acute hospital aquired pneumonias
Ca: Common- strep pneumoniae, Haemophilus influenza, klebsiella pneumoniae Atypical- chlamydia pneumophila, mycobacterium pneumoniae, legionella pneumophila Viral- influenza, RSV Ha- staph aureus, E. coli, pseudomonas aeriginosa, Immunosupression- pneumocystis jirovecii, candida, aspergillus, viruses
79
List the aetiological clues for the common respiratory tract pathogen
``` Strep pneumoniae- elderly, co morbid Aspiration - E. coli Legionella- travelling H influenzae - COPD Mycoplasma- young, prior antibiotics, extra pulmonary involvement S aureus- drug user, post viral ```
80
Clinical features of pneumonia
``` Malaise Fever Cough- productive, can vary in sputum Dyspnoea Chest pain on inspiration Chills, sweats rigors Vomiting Anorexia Myalgia Diarrhoea Wheeze ``` Dull on percussion Ausculation- crackles, wheeze, bronchial breath sounds
81
Investigations of pneumonia
CXR | Culture/ labs see other card
82
How do you assess the severity of pneumonia/ management?
``` Confusion urea >7 Resp rate over 30 Blood pressure less than 90 or 60 65 + 2+ = hospital 3+ = ICU ```
83
Understand the principles of collection of specimens for lab diagnosis of pneumoniae
``` Nose/ throat swab Sputum sample- bronchial/alveolar lavage Biopsy? Blood Urine- legionella Serotyping ``` Microscopy Macroscopic - sputum Culture- stain acid and alcohol fast Antibody/ antigen detection
84
Common opportunistic pneumonia infections
Pneumocystis spp. Aspiration e.g. Coma, alcoholics, epilepsy, dysphagia - E. coli and pseudomonas Whooping cough- bordetella pertussis- culture and PCR, cough and vomit, erythromycin Aspergillus and candida Cytomegalovirus Cryptosporidium Protozoa Mycobacterium spp. CF- haemophilus, s aureus, later pseudomonas auringinosa.
85
Describe the principles of anti microbial therapy in pneumonia and understand the rationale for selecting different antibiotics
Pneumococcus- amoxicillin or if severe then co-amoxiclav | If atypical then erythromycin,clarithromycin, doxycycline, levofloxacin for legionella.
86
Describe the microbiology of mycobacterium tuberculosis
Acid and alcohol fast bacilli. | Spread via aerosol
87
Describe the pathology of m tuberculosis
Acute- forms primary complex- sub pleural lesions Ghon's focus and infects hilar lymph nodes. When they occur together they are called the primary complex. Can calico fly or spread. Post primary infection - beyond first week, throughout body/ lung military spread. Cavitation of lungs and cytokines mediated systemic effects. Spread to kidneys, limbo sacral spine, large joints, meningitis.
88
Describe the host response to a TB infection
Ingested by macrophage but prevents fusion of phagosome with lysosomes. Escapes and multiplies in cytoplasm. Provokes immune response - il2 then IFn-g and TNF a. Activate and recruit more macrophages causing granulomas
89
Describe the typical presentation and radiographic changes in resp TB
``` Dyspnoea Cough- wet or dry Haemoptysis Fever Primary - asymptomatic Tiredness and malaise Weight loss and anorexia. ``` Non specific signs, palor, fever, weigtloss, clubbing, lymph nodes X ray changes - shadowing, cavities, consolidation, military seeds, Cardiomegaly, calcification.
90
Describe the primary and post primary changes in TB
Primary - swollen lymph possible | Post primary - symptoms especially cough, fevers and weight loss.
91
Describe lymph TB
Affects neck- internal thoracic, swollen, inflamed, may compress trachea/ bronchi
92
Describe orthopaedic TB
Spondylitis- sub chondral ossification along lateral ligaments - paraplegia and quadriplegia possible Poncets disease- poly arthritis
93
Describe meningitis from TB
Headache, fever, confusion coma. | Normally from military TB
94
Describe pleural TB
Hypersensitivity response in primary infection Or Tuberculous Empyema with ruptured cavity through chest wall.
95
Describe miliary TB
Bacilli in blood from primary or reactivation. | Spread to multiple organs/ sites within lungs.
97
Diagnosis of TB
Clinical features CXR Sputum sampling- swab/ lavage, blood culture, biopsy
97
Describe the mechanisms of drug resistance in TB
Spontaneous mutations. | Poor adherence means multi drug resistant TB (mdrtb) increasing.
98
Describe the management of TB and side effects
Rifamipicin- hepatitis, rash, flu like symptoms, ARF, thrombocytopenic purpura Isoniazid- hepatitis, rash, peripheral neuropathy Pyrazinamide - hepatitis, rash, arthralgia Ethambutol- optic neuritis 4 then 2 2 months and 6 months Only infectious for 2 weeks Poor adherence
99
Describe the BCG
Uses live attenuated bovine tuberculosis bacillus. Lasts 15 years. Variable efficacy. Used for high risk groups
100
High risk groups TB
``` HIV Corticosteroids or anti TNF antibody Immunosuppressant Post surgery Silicosis Malnutrition IV drug Overcrowding Smokers and chronic lung disease Asians Diabetes ```
101
Describe the relationship between TB and HIV
Leading cause of death in HIV patients. | Much higher risk
102
Describe public health issues surrounding a case of TB
Immediate contact with TB radiology if suspected and treatment started immediately
103
Describe the incidence of lung cancer in different groups
Men 100 in 100000 mortality vs 40 in women Linked to socioeconomic factors Increasing in women and decreasing in men
104
Give an account of the aetiological factors involved in lung cancer
``` Smoking - most Radon Genetics Asbestos Diet ```
105
Describe the typical pattern of symptoms reported by patients with lung cancer
Primary- Haemoptysis, Dyspnoea, cough, chest pain, wheezing, post obstructive pneumonia Regional mets- hoarseness, Dyspnoea - phrenic nerve, SVC obstruction, dysphagia Distant mets - bone pain fractures, CNS features, vision, headache, confusion ect. .
106
Where can lung cancer spread?
Brain, lymph, pericardium, lung, pleura. Liver, adrenals, bone
107
Describe common paraneoplastic syndromes associated with lung cancer and understand the structural abnormalities underlying them
Paraneoplastic- endocrine cushings,SIADH, hypercalcaemia Neurological - encephalopathy, peripheral neuropathy, eaton-lambert syndrome Anaemia, thrombocytosis, clubbin
108
Common methods used to obtain material for histological diagnosis
Histological diagnosis necessary for cell type and prognosis Bronchoscopy Needle biopsy Thoracocentesis
109
Diagnosis and staging of lung cancer
Initially CXR Serum biochemistry Imagining with ct, isotope bone scan, bronchoscopy Tissue with biopsy
110
Give an account of he histology and classification of common lung tumours
Non small cell: Squamous cell carcinoma (40%) - central angulate cells, eosinophilic, keratinisation (pearls) Adenocarcinoma 35%- peripheral tumours, columnar/ cuboidal cells, acini, papillary structures, May line alveoli, may produce mucins Large cell carcinoma Small cell carcinoma 12%- less cytoplasm, small nuclei, nuclear moulding, necrosis and mitosis. Oat cell carcinoma
111
Behaviour of different cancer and prognosis and treatment
Most non small cell are inoperable but most small cell are metastatic so has a worse prognosis.
112
Different treatments for lung cancer
Surgery for NSS Chemotherapy, potentially curative in NSS and can lead to improvements in SS Radiotherapy- radical or palliative Biological therapies- EGFR, immunotherapy Combination therapy Palliative care
113
Describe pleural effusion, pneumothorax, consolidation, space occupying lesion, lung collapse
Pneumothorax- black air trapped, visible pleural edge, tracheal shift away Pleural effusion- loss of costs phrenic angles of hemidiaphragm, meniscus of fluid Consolidation- dense opacification SOL- nodule less than 3, mass larger. Causes malignancy, inflammation, congenital, benign mass legion Lung collapse- elevation of hemidiaphragm, crowding of ribs, shift of mediastinum towards, crowding of pulmonary vessels, sail sign
114
Identify cardiac enlargement/ cardiac index
PA | Ratio of heart to rib age at largest. Normal is below 50%
115
Causes of ILS
Immunological - sarcoidosis- steroids, may be obstruction too Connective tissue disorder- RA, SLE, scleroderma, polymyositis Occupational- coal workers, farmers - extrinsic allergic alveolitis e.g. Bird fanciers lung, farmers, asbestososis Idiopathic (50%)- IPF steroids, IIP no treatment Treatment related- methotrexate, amioderone, nitroflurotoin, chemotherapy
116
Describe the involvement of different inflam cells in interstitial lung disease
Area inbetween air spaces for support, diffusion and repair | Epithelial, endothelial, macrophages, mesenchymal and other inflam cells
117
Clinical features of ILS.
SOB, reduced exercise tolerance, dry cough Tachpnoea, tachycardia,reduced chest movements, coarse crackles, cyanosis, RHF, clubbing in CFA(crypto genic fibrosing alveolitis) Restrictive
118
Effect on gas exchange
Reduced transfer factor Fibrosis so dead space Less compliance Increased diffusion pathway
119
Lung function tests of ILS
Restrictive so decreased FVC
120
Lung diseases and occupations ILS
Diffuse fibrosis- asbestosis is Modular fibrosis- pneumoconiosis, duct, silica, asbestos Alveolitis- farmer, pigeon
121
Xray of ILS
Fibrosing alveolitis - small, micro modular shadowing, ragged heart boarder Extrinsic allergic alv - acute micro nodules, chronic is almost normal then disease Sarcoidosis- military modular shadowing, diffuse fibrosis Asbestosis is- plaques, fibrosis, mesothelioma
122
Factors affecting formation and reabsorption of pleural fluid
Production of absorption failure Production- increase in pressure, increase in interstitial fluid, increase in permeability e.g. Infection or malignancy, decrease in oncotic Absorption- increase in BP, lymph blockage
123
Types of pleural effusion
Haemothorax Chylothorax (lipid) Empyema (pus) Simple effusion (serous fluid)
124
Transudate / exudate
30g/litre Transudate- difference in starling forces Exudate- dilation or vasculature or leakage
125
Describe the characteristics and causes of pleurisy
``` Chest pain- if diaphragm then shoulder Pain on inspiration, cough, sneeze, laugh Small breaths Pleural rub can be heard Causes Autoimmune - RA, SLE Infection Cancer- mesothelioma (asbestos) Pneumothorax PE Unabsorbed effusion Can lead to pleural fibrosis ```
126
Describe chest wall abnormalities and motor/ neurological diseases that can affect breathing
Pertussis carcinatum and excavatum, kyphosis, scoliosis. Acquired deformities. Muscular dystrophy, Motor neurone disease, polio
127
Course of the oblique fisssures
T2 SP- anterior behind 6 costal cartilage
128
Course of the right horizontal fissure
4th rib from MAL to anterior edge

Esa 3 (5 decks)

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